scholarly journals Physiological Effect of Ghrelin on Body Systems

2020 ◽  
Vol 2020 ◽  
pp. 1-26
Author(s):  
Yonas Akalu ◽  
Meseret Derbew Molla ◽  
Gashaw Dessie ◽  
Birhanu Ayelign
Keyword(s):  
Lung Development ◽  
Adrenocorticotropic Hormone ◽  
Molecular Mechanisms ◽  
Fetal Lung ◽  
Physiological Effect ◽  
The Body ◽  
Clear Understanding ◽  
Future Studies ◽  
Therapeutic Implications ◽  
Fetal Lung Development

Ghrelin is a relatively novel multifaceted hormone that has been found to exert a plethora of physiological effects. In this review, we found/confirmed that ghrelin has effect on all body systems. It induces appetite; promotes the use of carbohydrates as a source of fuel while sparing fat; inhibits lipid oxidation and promotes lipogenesis; stimulates the gastric acid secretion and motility; improves cardiac performance; decreases blood pressure; and protects the kidneys, heart, and brain. Ghrelin is important for learning, memory, cognition, reward, sleep, taste sensation, olfaction, and sniffing. It has sympatholytic, analgesic, antimicrobial, antifibrotic, and osteogenic effects. Moreover, ghrelin makes the skeletal muscle more excitable and stimulates its regeneration following injury; delays puberty; promotes fetal lung development; decreases thyroid hormone and testosterone; stimulates release of growth hormone, prolactin, glucagon, adrenocorticotropic hormone, cortisol, vasopressin, and oxytocin; inhibits insulin release; and promotes wound healing. Ghrelin protects the body by different mechanisms including inhibition of unwanted inflammation and induction of autophagy. Having a clear understanding of the ghrelin effect in each system has therapeutic implications. Future studies are necessary to elucidate the molecular mechanisms of ghrelin actions as well as its application as a GHSR agonist to treat most common diseases in each system without any paradoxical outcomes on the other systems.

Fetal lung development via quantitative biomarkers from diffusion MRI and histological validation in rhesus macaques

2021 ◽  
Author(s):  
Nara S. Higano ◽  
Xuefeng Cao ◽  
Jinbang Guo ◽  
Xiaojie Wang ◽  
Christopher D. Kroenke ◽  
...  
Keyword(s):  
Lung Development ◽  
Diffusion Mri ◽  
Rhesus Macaques ◽  
Fetal Lung ◽  
Fetal Lung Development ◽  
Histological Validation

scholarly journals In utero administration of GABA promotes fetal lung development

2010 ◽  
Vol 24 (S1) ◽  
Author(s):  
Narendranath Reddy Chintagari ◽  
Yang Wang ◽  
Dong Xi ◽  
Lin Liu
Keyword(s):  
Lung Development ◽  
Fetal Lung ◽  
In Utero ◽  
Fetal Lung Development

scholarly journals MicroRNA-127 modulates fetal lung development

2009 ◽  
Vol 37 (3) ◽  
pp. 268-278 ◽  
Author(s):  
Manoj Bhaskaran ◽  
Yang Wang ◽  
Honghao Zhang ◽  
Tingting Weng ◽  
Pradyumna Baviskar ◽  
...  
Keyword(s):  
Expression Pattern ◽  
Lung Development ◽  
Fetal Lung ◽  
Mirna Microarray ◽  
Mirna Expression Pattern ◽  
Opposite Trend ◽  
Fetal Lung Development ◽  
Terminal Bud ◽  
Lung Organ Culture

MicroRNAs (miRNAs) are small endogenous RNAs and are widely regarded as one of the most important regulators of gene expression in both plants and animals. To define the roles of miRNAs in fetal lung development, we profiled the miRNA expression pattern during lung development with a miRNA microarray. We identified 21 miRNAs that showed significant changes in expression during lung development. These miRNAs were grouped into four distinct clusters based on their expression pattern. Cluster 1 contained miRNAs whose expression increased as development progressed, while clusters 2 and 3 showed the opposite trend of expression. miRNAs in cluster 4 including miRNA-127 (miR-127) had the highest expression at the late stage of fetal lung development. Quantitative real-time PCR validated the microarray results of six selected miRNAs. In situ hybridization demonstrated that miR-127 expression gradually shifted from mesenchymal cells to epithelial cells as development progressed. Overexpression of miR-127 in fetal lung organ culture significantly decreased the terminal bud count, increased terminal and internal bud sizes, and caused unevenness in bud sizes, indicating improper development. These findings suggest that miR-127 may have an important role in fetal lung development.

Glucocorticoids upregulate tropoelastin expression during late stages of fetal lung development

1995 ◽  
Vol 268 (3) ◽  
pp. L491-L500 ◽  
Author(s):  
R. A. Pierce ◽  
W. I. Mariencheck ◽  
S. Sandefur ◽  
E. C. Crouch ◽  
W. C. Parks
Keyword(s):  
Lung Development ◽  
Matrix Protein ◽  
Fetal Lung ◽  
Extracellular Matrix Protein ◽  
Transferase Activity ◽  
Mrna Levels ◽  
Pregnant Rats ◽  
Fetal Lung Development ◽  
Chloramphenicol Acetyl Transferase Activity

The production of elastin, an essential extracellular matrix protein of terminal airway interstitium, occurs mostly during early development. Because glucocorticoids influence airway maturation, we studied the effect of dexamethasone (Dex) on tropoelastin expression during fetal lung development. Timed-pregnant rats were treated with Dex (1 mg/kg daily), and fetal lungs were collected 3 days later at 17, 19, and 21 days of gestation. Dex treatment resulted in about a threefold increase in tropoelastin mRNA levels at 19 days concomitant with accelerated airway development. By in situ hybridization, Dex treatment increased the number of tropoelastin-expressing cells and the level of tropoelastin mRNA per cell. In organ culture, Dex increased lung tropoelastin expression and augmented cortisol stimulation of tropoelastin expression. In fetal pulmonary artery smooth muscle cells, 10(-8) M Dex upregulated tropoelastin mRNA expression and increased tropoelastin promoter-chloramphenicol acetyl transferase activity in transient transfections. These data indicate that pharmacologically administered glucocorticoids transcriptionally upregulate fetal lung tropoelastin expression and suggest that steroid hormones may be important regulators of elastin production in vivo.

The Biochemistry of Fetal Lung Development

1987 ◽  
Vol 14 (3) ◽  
pp. 481-507 ◽  
Author(s):  
Mitchell J. Kresch ◽  
Ian Gross
Keyword(s):  
Lung Development ◽  
Fetal Lung ◽  
Fetal Lung Development
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